Non-Hodgkins Lymphoma

risk factor Elderly Men Predisposed: primary and secondary immunodeficiency states – HIV infection – Undergone organ transplantation – With inherited immune deficiencies – Sicca syndromes

etiology Infectious agents – HTLV-1: adult T cell lymphoma – EBV: Burkitt’s lymphoma, primary CNS lymphoma, extranodal nasal T/NK cell lymphoma, aggressive non-Hodgkin’s lymphoma – HIV: aggressive B cell non-Hodgkin’s lymphoma – H. pylori: gastric MALT lymphoma – Borrelia sp.: skin MALT lymphoma – Chlamydophilia psittaci: eyes MALT lymphoma – C. jejuni: small intestine MALT lymphoma – Hepatitis C virus: lymphoplasmacytic lymphoma – Human herpes virus 8: primary effusion lymphoma, multicentric Castleman’s disease

etiology Chemical exposures – Exposure to agriculture chemicals  increase incidence of non-Hodgkins lymphoma Medical treatment – Patients treated for Hodgkin’s disease

immunology Majority are of B cell in origin Stage of differentiation does not predict the natural history Immunologic cell surface phenotype of more primitive cells are less aggressive and more amenable to curative therapy Apparent stage of differentiation does not reflect the stage at which the genetic lesions that gave rise to the malignancy developed

Cell surface phenotyping is to aid in the differential diagnosis of lymphoid tumors that appear similar by light microscopy Malignancies of lymphoid cells are associated with recurring genetic abnormalities and can be identified at variety of levels: – Gross chromosomal change – Rearrangement of specific genes – Overexpression, underexpression, mutation of specific oncogenes

Gene profiling – simultaneous assessment of expression of thousand genes – Identify new genes with pathologic importance, patterns of gene expression with diagnostic/prognostic significance, new therapeutic targets